关于国外渗透性脱髓鞘综合征部分文献之重新分析：反思英文摘要与说明张海鹏 1，8，9 ，张 力 2，杜长生 3，陈宗羡 4，曾伏虎 4,5,翟所鑫 4，李玉清 1,刘庆梅 1,朱玉忠 1, 王荣明 8，杨子军 1，闫四梅 3，陈 萌 8，崔 松 91.涿鹿县医院/河北北方学院第七教学医院神经外科， 8普外科， 9放射医学与应用物理研究所，涿鹿桑干河075600；2.河北北方学院神经药理学系,张家口075000；3.中国人民武警部队总医院脑系科，北京100039；4.河北北方学院第二附属医院脑系科，张家口075100；5.佛山市南海区第二人民医院，广东528251；6.东营市鸿港医院神经内科，山东257061；7.华北石油总医院神经内科，河北062500（通讯作者：张海鹏，e-mail: heapprenzcomhard163.com;张力，e-mail:zmczl hotmail.com）Something Related to the Beriberi Secondary to Hepatic Transplantation,the Hypokalemic Non-periodic Paralysis or the Encephalopathy of Alkalosis: A Primary Reretro-consideration on Some International Documentations Concerning the “Osmotic Demyelination Syndrome”Seeming to Include Central Pontine MyelinolysisZhang Hai-peng 1,8,9, Zhang Li2, Du Chang-sheng 3 ,Chen Zong-xian4, Zeng Fu-hu4,5,Zhai Suo-xin4, Li Yu-qing1, Liu Qing-mei1, Zhu Yu-zhong1, Wang Rong-ming8, Yang Zi-jun 1, Yan Si-mei3, Chen Meng6,Cui Song7 1. Department of Neurosurgery， 8Department of General Surgery or 9Institute of Radiation Medicine and Applied Physics，Zhuolu-county Hospital & The 7th Teach-learning Hospital of Hebei North University, Sanggan-river,Zhuolu, Zhangjiakou 075600, Hebei, China;2.Department of Neuropharmacology, Hebei North University ,Zhangjiakou075000, Hebei, China;3.Department of Neurology, General Hospital of the Peoples Armed Police Forces of China, Beijing100039, China;4.Department of Neurology,The 2nd Hospital Attached to Hebei North Uni versity ,Zhangjiakou075100, Hebei, China; 5.The peoples 2nd Hospital of the Nanhai District of Foshan City ,Guangdong528251, China;6.Department of Neurology,Hong-gang Hospital of Dongying City,Shandong257061, China; 7.Department of Neurology,General Hospital of Oilfield in Northern China,Hebei062500, China.The authors answerable for the article: Zhang Hai-peng,e-mail: heapprenzcomhard163.com;Zhang Li，e-mail:zmczl hotmail.comAbstract Objectives: To explore the main etiological factors of central pontine myelinolysis (CPM) and of the “osmotic demyelination syndrome(ODS)”that occurs after hepatic transplantation, to explore the differential diagnosing the manifestation consisting of dysarthria, dysphagia and quadriplegia presented after vomiting for a number of times ,and to explore which fraction to be mainly involved by the “ODS” ,what to be the pathological mechanism of the “ODS” ,and how to prevent the “ODS”.Methods:Physiopathological principles are applied on the base of the clinical certificates ,the diagnostic results differring from those in the case reports (that have been analyzed again by us).Results and conclusions:It could be suggested that (1) CPM based mainly on alcoholism should result mainly from beriberi，as was mentioned by HUANG Ke-wei ,the well-known Chinese neurologist , before or in 1960;(2) The coma secondary to hepatic transplantation could be often caused by Wernicke encephalopathy(WE, one of beriberi),which could be asscociated with the postoperative elevated corticosteroid or/and high-starch food for liver cirrhosis ,which complicated by hepatic encephalopathy;(3)The case that was in 1995 reported by Kabeer et al，of possiblity of the earliest reported CPM due to cyclosporine，appeared to be the bilateral type of pontine lower paracentral hematal syndrome，a bilateral uncomplete Foville syndrome.It should be considerable whether an epileptic attack related to both cyclosporine and corticosteroid could result from reverible posterior leukoencephalopath syndrome with negative MRI owing to the effect of corticosteroid; (4) It is cerebral cortex that could be mainly involved by the “ODS” following a number of times of vomiting ,of which one of evidences has been the 2 cases reported by Tomlinson et al in 1976.The kind of “ODS” following the encephalopathy of alkalosis yet without hypoxemic hypoxia,is possibly preventable not only if the correction of hypokalemia is firstly comsidered and also if corticosteroid(for 3 days or shorter) is preventivly applied before correction of hyponatremia(0.9%NaCl,via digestive tract). Dose -filled vitamin B1 (i.m.) ，however,ought to be given so as not to induce beriberi including CPM before corticosteroid is used;(5) The hypokalemia caused by vomiting and alkalosis thereof ,can maybe account for dysarthria, dysphagia and quadriplegia,when there is not obvious difference between the severity of bulbar paralysis and that of quadriplegia ;and quadriceps reflex often plays down in patient with hypokalemic non-periodic paralysis（HNP）.Thereby,each of some reported cases with (clinical)CPM ,including several of 22 ones reported by Heng ,et al(2007) ,the one by Shintani, et al(2005) and the one by Bhr,et al(1990) ,has shown itself rather as sub-clinical CPM (with HNP) than clinical CPM (without HNP) suggested only by MRI.(6)It is supposed that why for CPM to involve the pyramidal tract inside pone, could be based on that the pontine paracentral branch of basilar artery had tended to “degeneration”in a limite